Elevated levels of SAA are down-regulated by therapy with PPARγagonist agents [19,23], whereas glucocorticoidtreatment did not downregulate extrahepatic expression of SAA [11,24,25].In chronic inflammatory diseases, such as rheumatoid arthritis, metabolic syndrome oratherosclerosis, prolonged elevation of SAA may contribute to tissue damage anddegradation [26–28]. The gene discussed is SAA1; the disease is metabolic syndrome.